Ventilation Mechanics Flashcards
Transpulmonary pressure
Difference between the alveolar and pleural pressures
- pleural pressures are determined via the esophagus
Compliance
(Difference in volume from two points / difference of pressures from two points)
Also can be measured by then slope between two points on a transpulmonary pressure vs lung volume graphs
- steeper the slope, greater the compliance
Effects of emphysema and fibrosis on lung compliance
Emphysema
- increases the lung compliance beyond normal values
- also increases the FRC of the lungs
- is an obstructive Lung disease, causes increased stagnant volume of air since it is an exhalation dysfunction
Fibrosis
- decreases the lung compliance beyond normal values
- also decreases the FRC of the lungs
- is a restrictive lung disease, causes decreased stagnant volume of air since it is an inhalation dysfunction
Which part of the breathing cycle has the higher compliance?
Deflation (exhalation)
- this is due to surfactant
What is the normal (quiet) breathing cycles normal TLC range?
50-60%
Hysteresis
Changes in the physical properties of the body due to changes in the forces
- quiet breathing has less hysteresis than forced breathing
Effect of surface tension on compliance
Increases in compliance
- compliance slope gets steeper, since the walls cannot stick with each other
note that liquid increases compliance more than air does
Pulmonary surfactant consists of what
Lipids
Dipalmitoylphosphatidylcholine (DPPC)
Apoproteins
What cells create surfactant?
Type 2 alveolar cells
Surfactant generation
Occurs usually around week 24 of infancy, but is almost always done by week 35
Requires a DPPC: sphingomyelin ratio of 2:1 or higher
- this ratio indicates mature surfactant production
Decreases surface tension in the lungs, increasing compliance
Neonatal respiratory distress syndrome
Occurs in premature infants whose surfactant is nor being produced on a mature level
Produces atelectasis, decreased compliance, hypoxemia
Law of Laplace for a sphere equation
P = 2T/r
P = collapsing pressure
T = tension of the sphere
R = radius of the sphere
- used for the respiratory and circulatory system to describe the relationship of collapsing pressure to radius*
- note that this equation suggests smaller alveolus have higher collapsing pressures (want to collapse), but dont in normal people due to surfactant prescience *
When is the system at functional residual capacity
At rest (no inspiration of expiration)
Changes in pressures and the respiratory system during inspiration
Inspiration muscles contract and chest expands
- increases volume in the chest and alveoli
- decreases pressures in the alveoli below the atmospheric pressure (lower than 760mmHg, usually 759mmHg), allowing air to move into the alveoli
Changes in pressures and the respiratory system during expiration
Inspiratory muscles relax, decreasing chest volume and increasing the pressures in the alveoli and lungs (above 760mmHg, usually 761mmHg)
Causes collapsing of the alveoli and air leaves back into the system from the lung
Principles Muscles of inspiration
External intercostals
Internal intercostals
Diaphragm
Accessory muscles of inspiration
SCM
Scalenes
Trans mural pressure
((Alveolar pressure) - (intrapleural pressure))
Does atmospheric/barometric pressures change during breathing?
No .
Intrapleural pressure
Pressure in the lungs at any time
At rest, hovers around -5cmHg
Gets more negative in inspiration and more positive (but not past -5cmHg) during expiration
Changes in volume, intrapleural pressure and alveolar pressures during the respiratory cycle
Inhalation:
- volume goes up (max is 500ml)
- intrapleural pressure goes down (usually around -8 H20cm)
- alveolar pressure goes more negative at the inspiration peak
Expiration:
- volume goes down to baseline
- intrapleural pressure goes back to baseline (from -8 -> -5)
- alveolar pressure becomes more positive at the peak of expiration
Airflow relationship between alveolar pressure, atmospheric pressure and airway resistance
Directly proportional
- alveolar and atmospheric pressures
Inversely proportional
- airway resistance
What does COPD do to airway resistance
Increases the resistance in all airways except in the pharynx/larynx
Increases are most apparent in the SMALLER airways
Lung volume differences in restrictive lung diseases
Residual volume (RV) = down
Functional residual capacity (FRC) = down
Total Lung Capacity (TLC) = down
Forced Vital Capacity (FVC) = 2x down
Forced Expiratory Volume (FEV) = down
FEV/FVC ratio = up or normal
- examples are pulmonary fibrosis*
Lung volume differences in obstructive Lung diseases
Residual volume (RV) = 2x up
Functional residual capacity (FRC) = up
Total Lung Capacity (TLC) = up
Forced Vital Capacity (FVC) = down
Forced Expiratory Volume (FEV) = 2x down
FEV/FVC ratio = down
examples are emphysema, chronic bronchitis, asthma, COPD
Why does the FEV and FVC decrease in the amount of air that can be pushed out of the lungs during obstructive lung diseases?
Two reasons
1)The transpulmonary pressure in the alveoli of obstructive disorders is less positive, so less oxygen moves in and out
2) the bronchioles will collapse due to inverted transpulmonary pressure gradient in the bronchioles, causing less air to be expired.
- this generates high resistance
What is a normal FEV1/FVC ratio?
- 8 or 80%
* note the ratio can also be shown as FEV1%, it means the same thing*
Why do people with emphysema breath w/ purse lips?
To maintain a positive end-expiratory pressure (PEEP)
- prevents bronchiole collapsing
How do maximal expiration flow volume loops change w/ obstructive and restrictive lung diseases?
Obstructive
- loop “shifts to left”
- RV goes up
- TLC goes down
- FVC goes down
- will show a dip in the curve in expiration if patients bronchioles are collapsing
Restrictive
- loop “shifts to right”
- RV goes down
- TLC goes down
- FVC goes down
What factors/substances in venous blood does the lungs filter out?
Prostaglandins E only (NOT A)
Leukotrienes
Serotonin (95%)
Norepinephrine (30%)
Bradykinin (80%)
Angiotensin 1
- is not removed but just activated to angiotensin 2
ATP (90%)
Endothelin-1 (50%)
Residual volume (RV)
Amount of air left in the lung after forced expiration
- normal volume usually is around 1.5-2L
CANT be measured, only is estimated via other measurements
Total lung capacity (TLC)
Total amount of air in the lungs altogether with full inspiration
- normal levels are 5-6L
IRV + TV + ERV + RV
OR
FRC + IC
Inspiratory reserve volume (IRV)
The difference in amount of air in lungs after forced inspiration vs quiet inspiration
- normal levels are 2-2.5L
Tidal volume (TV)
Difference of volume between quiet inspiration and expiration
- normal breathing cycle
- normal levels are around 0.5L
Expiratory reserve volume (ERV)
The volume difference between quiet expiration and forced expiration
- normal levels are usually around 1-1.5L
Inspiratory capacity (IC)
Difference in volume form quiet exhalation -> forced inhalation
- normal levels are usually 2-3L
Tidal volume (TV) + Inspiratory reserve volume (IRV)
Functional residual capacity (FRC)
Difference in volume from quiet expiration -> TLC
- normal levels are around 2.5-3.5L
Expiratory reserve volume (ERV) + Residual volume (RV)
Vital capacity (VC)
Difference in total volume in lungs after forced inspiration and volume in lungs after forced expiration
- normal volume is usually 3.5-4.5
- Inspiratory Capacity (IC) + Expiratory Reserve Volume (ERV)*
Forced Expiratory volume (FEV1)
Amount of air forced out after forced inhalation with forced exhalation in the first second
- important volume to measure
What are ways to try and measure residual volume?
Nitrogen-washout
Plethysmograph
Helium-dilution
If there is a zero on a pressure graphic for pulmonologist, does that mean the pressure is truly zero?
NO
All pressures on graphics are with respect to 760mmHg barometric pressure
ex: -5 = 755mmHg
Transpulmonary pressure (PTP)
Determines the pressure difference across the lung wall
alveolar pressure (Pa) - intrapleural pressure (Pip)
- if PTP > 0 = Alveoli are open*
- if PTP < or equal to 0 = Alveoli are closed*
- atelectasis
- under normal resting conditions, PTP = +5*
- 0 - -5 = +5
How does PTP change during pneumunothroax?
Goes to zero, which causes alveoli to remain shut and cannot open properly
- causes atelectasis
Fixes by pushing air into the lungs (positive airway pressure)
Hypoxia pulmonary vasoconstriction (HPV)
Pulmonary vascular resistance increases in response to hypoxia (20-40 min)
- this vasoconstriction occurs due to increased cytosolic calcium as a result from hypoxia
Minute ventilation
Amount of ventilating during 1 minute
- it ignores the deadspace air that is always prevalent in the conducting zone
Is calculated by Tidal volume (500 mL) x RR
Dead space ventilation (VD)
Volume of space in conducting zone at anytime during ventilation in 1 minute
- dead space volume (VD) * frequency of breathing (RR)
(.15L) x (12) = 1.8L
Alveolar ventilation (VA)
Amount of air going into the alveoli in 1 minute
Equal to (tidal volume - dead space ventilation) x RR
- alveolar ventilation is inversely proportional to amount of dead space ventilation*
How to calculate physiological dead space (Bohr method)
VD = VT * ((PaCO2 - PECO2) / (PaCO2))
VT = tidal volume
PECO2 = CO2 expired
PaCO2 = partial pressure of CO2
CO2 expired is inversely proportional to Physiological dead space
What is the relationship between alveolar and arterial PACO2 to alveolar ventilation?
Inversely proportional
Alveolar ventilation equation
VA = 0.863 * (VCO2/PACO2)
VCO2 = total carbon dioxide production
- can flip the equation to show PACO2 = 0.863 * (VCO2/VA)*
What is the relationship between alveolar PCO2 and arterial PCO2?
They are equal to each other
What is the relationship between alveolar PO2 and arterial PO2?
Nn
How do you calculate PAO2?
Calculated through the alveolar gas equation
* PAO2 = PIO2 - (PACO/RQ)*
* also can be simplified to the following as long as normal conditions w/ western are met:
PAO2 = 150 - 1.25(PaCO2)*
RQ = respiratory quotient and calculated by: RQ = (VCO2/VO2)
- this is normally around 0.8 in a western diet
- protein based diet causes it to increase
- fat based diet causes it to decrease
What is RQ in the alveolar gas equation?
RQ = respiratory quotient and calculated by: RQ = (VCO2/VO2)
- this is normally around 0.8 in a western diet
- protein based diet causes it to increase
- fat based diet causes it to decrease
How does the alveolar ventilation change as you move from the base of the lung to the apex?
Decreases, but dramatically
- due to gravity
- also same with perfusion
- V/Q ratio is increased at the apex of the lung however
Does the systemic or the pulmonary capillaries have more area?
Pulmonary
Difference of vascular resistance in all types of pulmonary blood vessels at RV, FRC and TLC?
Alveolar blood vessels RV = lowest point FRC = medium point TLC = highest point - as lungs inflate, resistance goes UP
Extra-alveolar blood vessels RV = highest point FRC = medium point TLC = lowest point - as lungs inflate, resistance goes DOWN
together (total resistance) the lowest resistance in the pulmonary system is seen at the FRC w/ the highest at residual volume
How do vessels change as perfusion pressure increases?
Go through recruitment (vessels that were collapsed are now opening) and distention (vessels that weren’t collapsed now become wider)
How does hypoxia affect blood flow
Hypoxia is a strong vasoconstrictor
- this is caused by peaking calcium intracellularly and not going back to SR during hypoxia
V/Q mismatches create what in the pulmonary system
Hypoxia conditions and acidosis
Sometimes alkalosis also
High V/Q shows what with partial pressures?
High PO2
Low PCO2
Causes alkalosis
Low v/Q causes what with partial pressures?
PAO2 goes down
PACO2 goes up
Causes acidosis
Right to left shunt with respect to V/Q?
V/Q = 0
- PaO2 = 40
- PaCO2 = 46
- these are arterial values*
Causes partial pressures of oxygen and carbon dioxide in both veins and arteries to be equal.
Pulmonary embolism does what to V/Q?
Makes it go near to infinity
- PAO2 = 150
- PACO2 = 0
- these are alveoli measurements*
Causes of Hypoxia and why it causes hypoxia
1) decreased cardiac output
- causes hypoxia due to decreased blood flow
2) anemia
- causes hypoxia due to decreased hemoglobin concentration
3) carbon monoxide poisoning
- causes hypoxia due to shift to left of the sat curve (causing oxygen to not want to unbind to hemoglobin)
4) cyanide poisoning
- causes hypoxia due to tissues being unable to uptake oxygen
5) hypoxemia
- causes hypoxia due to decreased partial pressures of oxygen in blood
Causes of hypoxemia
1) High altitude
- no changes on A-a gradient
2) Hypo ventilation
- no changes on A-a gradient
3) V/Q defects
- increases A-a gradient
4) Right-left shunt
- increases A-a gradient
- only one that giving supplemental oxygen will not provide much benefit
5) Physical diffusion defects
- increases A-a gradient
What is the A-a gradient?
The difference of partial pressures oxygen between alveoli oxygen and arterial oxygen
- increases in A-a gradient implies that diffusion of oxygen is not working
normal A-a gradient is between 0-10
