Pulm Lectures; Exam II Flashcards
What happens if one side of the diaphragm is paralyzed?
Which lung is bigger and why?
-Heart sandwiched between the lungs
-Thorax contains the lungs and heart; consider this one sealed unit.
-If one side of the diaphragm is paralyzed, on inspiration the side that is not paralyzed will push down and the side that is paralyzed will be pushed upward
-R. lung is larger than the L. lung due to the space needed for the heart
-Lungs extend past rib 1, sometimes past the clavicle
How do the lungs move
Two sets of tissue that allow the lungs to move within the chest w/o friction
- Visceral pleura; outside of lungs
- Parietal pleura; stuck to visceral pleura, but on the side of the lungs
-On inspiration, lungs expand as the diaphragm contracts and pulls the lungs downward. This creates an even more negative pressure and causes air to be sucked in from the environment
Where is the diaphragm anchored?
-Anchored into the lumbar spine by two leaflets
What are we looking at here?
Inferior view of the diaphragm
- Caval canal; opening for the vena cava
- Esophageal aperture
- Aortic aperture
4.Central tendon; tendons are usually bone-bone. The central tendon is not connected to bone. Tendon in the middle of the diaphragm for the heart to sit on
What are we looking at here?
Anterior view of the diaphragm
- Esophageal aperture
- Caval aperture
- Central tendon
- Aortic Aperture
Phrenic nerves; run along the side of the neck, past the heart, and connect to the two sides of the diaphragm that they innervate
Only need one phrenic nerve to stay alive if we are completely healthy
Name the three sets of accessory muscles
What is being shown here?
Accessory muscles that help with ventilation during stress or exercise; scalene, intercostal, abdominal muscles
- Anterior Scalene; connect superiorly to C3-C6 and inferiorly to rib 1
- Middle Scalene; connect superiorly to C3-C7 and inferiorly to mid-rib 1
- Posterior Scalene; connect superiorly to C5-C7 and inferiorly to rib 2
Provide a platform to pull the ribcage up or pull the diaphragm down
In the circle is the top of the airway; the larynx. Contains the voicebox
1. Thyroid cartiledge
2. Cricoid cartiledge
3. R. Main stem
4. L. Mainstem
5. Tracheal bifurcation
6. Bronchioles continue to split until eventually becoming alveoli
24 generations of airways within the respiratory system
-Trachea is considered generation 0
-Should be 2cm in diameter
-mainstem bronchi are generation 1
-continue to split into bronchioles through generation 16
-This is the conducting zone; no ventilation happens here
-Generations 17-24 are our respirtatory/ventilation zone
-Respiratory bronchioles are transition zone; a small amount of gas exchange happens here due to a small number of alveoli (generations 17-19)
Alveoli have no cartiledge
- Normal
- Distress
- Not breathing
- Wheezing due to inflammation or tumor in airway
- Slow
- Fast
- Change in RR with position change
- Fast
- Ventilation that is occuring well in excess of metabolic demands
- Insufficient ventilation for metabolic demands
- Lungs that are larger than they should be. Ex; COPD. Connective tissue in lungs is lost, lungs expand too much
- DeoxyHgb >5gm/dL
- Decreased O2 at the level of the tissue
- Decreased O2 in the arterial system; systemic problem
- Excessive CO2 in arterial blood; hypercarbia
- Defiency of CO2 in arterial blood; hypocarbia
- O2 levels above normal at the tissue/organ level
- Collapse of functional lung units
- “P” 1mmHg = 1.36cmH2O
-using cmH2O gives us better resolution in the thoracic system - For our purposes; total O2 content of the blood = dissolved O2 and O2 attached to Hgb. How much gas content do we have in a sample?
- “a” PaO2
-“v” would be venous - “A” PAO2
- “V” how much air is moving in or out. Vt; tidal volume. Ve; expired volume of gas. Vi; gas going into the patient
- Volume of gas absorbed per minute; VO2; volume of O2 absorbed each minute. Indicated with a dot over the V
- Individual volumes of air
- Made up of individual volumes of air
- Stretch
- Inverse of compliance
-Total Lung Capacity: Sum total of volumes within the lung.
6L in a heathy adult, 3L per lung.
Total Lung Capacity contains the IRC, FRC, and the four volumes contained within those: **Inspiratory Capacity** 1. Inspiratory Reserve Volume (IRV): 2.5L. The volume of air that we can potentially inspire in addition to a normal Vt. 2. Tidal volume (Vt): 0.5L, volume of air moved during inspiration and expiration **Functional Residual Capacity** -(FRC) 3.0L. The volume of air remaining in the lungs after a normal, expired breath. Allows us to maintain stable blood gas levels, and prevents atelectasis in between breathes. 3. Expiratory Reserve Volume (ERV): 1.5L. The volume of air that we could push out of our lungs after expiration 4. Residual Volume (RV): 1.5L. Volume of air that we cannot expire from the lungs. Attempting to force this volume of air out would result in closing the airways.
-Vital Capacity (VC): 4.5L. The total amount of air that we can inspire and expire on maximal effort. Contains IRV, Vt, ERV
How do body position changes affect total lung capacity/pulmonary blood flow?
In a supine position; the weight from your abdomen will push your diaphragm upwards, causing air to be removed from the lungs.
Seated position: blood flow is still highest at the bottom
Supine: Blood flow is almost equal throughout, with flow being slightly higher at the apex. This is due to the apex of the lung being slightly head-down in this position
Normal Respiration
-This is a normal respiratory cycle that occurs over a period of four seconds
-Inspiratory and expiratory time are two seconds each
-One second in between breathes
-12 BPM is normal RR for this class
-Left side of graph is inspiration, right side is expiration
Vt, PIP, Air flow rate, and PA changes
Changes during inspiration
-In between breaths, our P IP is -5cmH2O
-During inspiration, the diaphragm pulls down on the lungs in a closed system, decreasing the P IP in order to suck air into the lungs.
-Vt steadily increases until the end of inspiration
-P IP decreases linearly over the course of two seconds during inspiration.
-At the end of inspiration, after we have inhaled our entire Vt, the P IP will decrease to -7.5cmH2O
-Air flow rate peaks halfway through inspiration (1 second) at 0.5L/sec. (The graph denotes inspired air as a negative number)
-Alveolar pressure is 0cmH2O in between breaths in comparison to the outside atmosphere (760cmH2O)
-During inspiration, the pressure surrounding the alveoli becomes more negative. (-5cmH2O –> -6cmH2) –> -7.5cmH2O)
-As this happens, the alveolar walls are being pulled open, causing the P A to decrease. This allows for air to be sucked into the lungs.
-As the air moves in, the pressure in alveoli begins to equilibrate with the environment. This is when inspiration ends
-Peak inspiration occurs when P A is at it’s lowest at -1cmH2O. This also corresponds to airflow rate being at it’s fastest.
Changes during expiration
-Vt decreases gradually through expiration
-P IP decreases linearly over the course of two seconds during expiration.
-P IP starts at -7.5cmH2O at the beginning of expiration
-Relaxing the diaphragm causes the P IP to go from -7.5cmH2O –> -6cmH2O –> -5cmH2O
-Air flow rate peaks halfway through expiration at 0.5L/sec (the graph denotes expiration as a positive number)
-Relaxing the diaphragm causes elastic recoil of the alveoli, making the P A to become more positive, and allowing for air to be pushed out of the lungs
-P A peaks halfway through expiration at +1cmH2O
-Pleural Pressure can be:
P IP or P PL
-Airflow rate will always be volume/time
-Transpulmonary Pressure: P TP
-Comparing pressures on two sides a wall (Delta P); pleural pressure vs alveolar pressure
West Perfusion Zones; Zone 1
- PA is greater than Pa & Pv
-Why does this happen? This is a continuous column of blood with a hydrostatic pressure gradient. The higher we move up the column, the higher the pressure becomes outside the capillaries, causing the alveolar capillaries to collapse.
- Compression of the capillaries
- Not seen under normal conditions in a healthy patient. Pa is just high enough to raise the blood to the top of the lungs
- When would this occur:
o Pa is reduced because of hemorrhage
o Positive pressure ventilation
West Perfusion Zones; Zone 2
- Pa is greater than PA, but PA is exceeding Pv
- Blood flow does not depend on the gradient (difference) between Pa and Pv at this point. Blood flow is dependent upon the gradient between Pa and PA.
o Why? Because the capillaries are collapsible. They collapse at the point where PA pressure exceeds Pv (start of the venous end of the capillaries)
o Often called the “waterfall effect” because the flow of a waterfall is not dependent upon the downstream pressure
- Why does this happen in this zone of the lung? Because Pa increases the further we move down the lung, but PA remains constant
Pulsatile blood flow
West Perfusion Zones; Zone 3
- Pa is increased even more, Pv is also increased because of the hydrostatic gradient, and PA now has the lowest pressure
- Capillaries are held open because of the increased Pa and Pv, and blood flow is determined with the usual formula. Pa-Pv
Continuous blood flow
Blood flow through the lungs is dependent upon what?
Gravity
What is zone 4?
The lower we are in the lung, the higher the blood flow
-In an upright patient, blood flow peaks and then decreases slightly
-This is due to the lungs sitting on top of the diaphgram. The blood vessels at the bottom of the lung can become compressed, decreasing blood flow
This refers to the alveolar vessels
PA and it’s affects on the pulmonary capillaries
If PA is greater than Pa or Pv, what happens?
-The PA directly affects the the pulmonary capillaries (alveolar vessels).
-Pulmonary capillaries are sitting within the walls of the alveoli.
-If alveolar pressure is higher than Pa or Pv, the capillaries will collapse.
-If Pa and Pv are greater than PA, the capillaries will remain open
-This is because the pulmonary capillary walls are very thin to allow for gas exchange, easily collapsible
When alveoli are full, what happens to the vessel walls?
PA and it’s affects on the extra-alveolar vessels
Alveoli/lung parenchyma pull on the walls of the extra-alveolar pulmonary veins and arteries, meaning that the pressure in these vessels should be lower than the pressure in the alveoli when they are full
How do these two factors decrease PVR? What causes this to happen?
Alveolar Capillary Recruitment and Distention
When you increase Pa or Pv, with the other pressure being held constant, the alveolar capillary pressure must increase because the capillaries are between the arteries and veins.
When you increase Pcap, two things happen:
1. Recruitment of capillaries; meaning capillaries open up and allow flow. “opening up” = PVR
-Under normal conditions, capillaries are closed or open, but with little to no flow
2. Distention; increase in the caliber of the capillaries, allowing the capillaries to become more circular in cross-section and increase flow. Dilating = decreased PVR
Bottom line: Increased pressure in the capillaries causes them to distend, increasing flow, and reducing PVR
Lung Volume and it’s affects on PVR
-If lung volume is reduced, PVR is increased. This is because the traction of the alveolar walls is decreased due to the decreased in volume, resulting in smaller capillaries –> increased PVR
-If lung volume is high, PVR is also increased. This is likely because the alveolar pressure is higher, distorting the vessels (almost like stretching out a rubber tube, it collapes)
Ptp throughout respiration
-
At Rest (End of Expiration, Before Inhalation):
P A = 0 cmH₂O (equal to atmospheric pressure)
Pip = -5 cmH₂O (slightly negative due to elastic recoil of the lungs)
Ptp = 0 - (-5) = +5 cmH₂O → Keeps alveoli open -
During Inspiration:
Diaphragm contracts, expanding the chest.
Pip becomes more negative (-8 cmH₂O), pulling lungs outward.
P A briefly drops ( -1 cmH₂O) to allow air to flow in.
Ptp increases (+7 cmH₂O), expanding the lungs further. -
At End-Inspiration:
P A returns to 0 cmH₂O (no airflow, pressure equilibrates).
Pip remains negative (-8 cmH₂O).
Ptp is highest (+8 cmH₂O), keeping alveoli maximally expanded. -
During Expiration:
Diaphragm relaxes, reducing chest volume.
Pip becomes less negative ( -5 cmH₂O).
P A briefly rises (+1 cmH₂O), pushing air out.
Ptp decreases (e.g., +6 cmH₂O), allowing lungs to recoil. -
Back to Rest (End of Expiration)
P A = 0 cmH₂O, Pip = -5 cmH₂O, Ptp = +5 cmH₂O (same as before inspiration).
Summary
Ptp is always positive (to keep lungs open).
Ptp increases during inspiration (as lungs expand).
Ptp decreases during expiration (as lungs recoil).
the force that does what? What happens as Ttp increases? & Decreases?
Transpulmonary Pressure
How does PPV affect Ttp?
- The pressure available to fill the lung up with air/distend the lung regardless of how the lung is being ventilated.
- Keeps the alveoli open
- As we increase transpulmonary pressure, more air gets pushed into the lung
- As we decrease transpulmonary pressure, air is pushed out of the lung
- PPV: Air is actively pushed into the lungs, increasing alveolar pressure (PA). Since pleural pressure (Ppl) does not become as negative (and may even become positive in high-pressure ventilation), the transpulmonary pressure increases more than in normal breathing
Total PVR
PVR and Lung Volume
Total PVR is equal to the sum of what?
-Lung volume passively effects PVR
-FRC is when PVR is consistently at it’s lowest.
-Increasing total lung volume = PVR Increases
-Decreasing total lung volume = PVR increases
-Consists of two components, alveolar and extra-alveolar blood vessels
-Total PVR is equal to the sum of alveolar vessel VR + extra-alveolar VR
Alveolar Blood Vessels
PVR and Lung Volume
What changes are taking place in the extra-alveolar vessels?
-Capillaries lining the alveoli
-Directly affected by alveolar pressure
Inspiration
-The higher the alveolar pressure/the more volume that the lung has–> the capillaries are pulled/stretched out and become longer & narrow –> alveolar VR is increased
-As this is happening, the walls of the extra-alveolar vessels are being pulled open, decreasing extra-alveolar VR
Expiration
-The lower the lung volume/alveolar pressure –> capillaries will become shorter & wider–> alveolar VR is decreased
-As this is happening, the walls of the extra-alveolar vessels are being pushed together, increasing extra-alveolar VR
Extra-alveolar blood vessel VR
PVR and Lung Volume
What changes are taking place with the alveolar vessel VR?
-Large vessels outside of the alveoli
-Directly effected by intrapleural pressure.
-Negative intrapleural pressure pulls the walls of the blood vessels apart
Inspiration
-The more negative the intrapleural pressure, the larger the diameter of the blood vessels will be; therefore, decreasing PVR
-As this is happening, alveolar pressure will be increasing, causing an increase in alveolar vessel resistance
Expiration
-The higher the intrapleural pressure, the more narrow the diameter of the extra-alveolar vessels will be, increasing PVR
-As this is happening, alveolar pressure will be decreasing, causing a decrease in alveolar vessel resistance
Alveolar VR, Extra-alveolar VR, and Total PVR
PPV & how that affects PVR
-PPV; using a positive pressure to increase lung volume. The positive pressure is pushing on the extra-alveolar blood vessels, increasing PVR while increasing lung volume
-Alveolar vessel capillary resistance will also increase due to the increase in volume, causing an increase in total PVR
Pulmonary blood flow depends on what factor?
Pulmonary Blood Flow & PVR
Distention vs Recruitment
How does decreased pulm blood flow affect the heart?
-Passive
-Pulmonary blood flow is dependent upon right heart cardiac output
-R. Heart CO increases –>
-PVR decreases because pulmonary capillaries distend to hold the additional volume.
-Recruitment of additional unused capillary pathways. This also decreases PVR
This process keeps the load on the right heart manageable as there is in increase in CO
-R. Heart CO decreases —>
-PVR increases as R. Heart CO decreases. Especially challenging on patients with conditions such as R. heart failure, massive R. sided MI
Interstitial P, Blood Viscosity, PPV
Passive Influences on PVR (Comprehensive List)
-Gravity, lung volume, pulmonary blood blow
-Increased interstitial Pressure
-Compression of vessels, increase in PVR
-Increase blood viscosity
-Viscosity is directly related to resistance
-PPV:
-Increased alveolar pressure: compression and derecruitment of alveolar vessels
-Positive intrapleural pressure: Compression of extra-alveolar vessels
All increase PVR with the exception of increased pulmonary blood flow
11 factors on this list
Active Influences on Increasing PVR
-Sympathetic stimulation:
-Process that constricts blood vessels out of the lungs in order to redistribute it elsewhere
-Epi, Norepi
-A. Adrengeric Agonists
-PGF 2a, PGE2
-Thromboxane
-Endothelin
-Both inflammatory agents that constrict pulmonary vessels
-Angiotensin
-Histamine (typically a vasodilator in systemic circuit)
-Venoconstricter in the lungs
-Alveolar hypoxia
-Alveolar hypercapnia
-Low pH in mixed venous blood
7 factors on this list
Active Influences on Decreasing PVR
-Parasympathetic stimulation
-Pulmonary vessels dilate, lungs become a reservoir for blood again
-Nitric Oxide
-Bradykinin
-ACh
-Dilates systemic & pulm vessels
-B. Adrengeric Agonists
-PGE1
-Prostacyclin (PGI2)
-Relaxes pulm vessels. Research done to use an inhaled gas mixture to treat pulm HTN
Atm P is? Partial pressure formula? 2 factors needed to get gas inbody
Partial Pressures of Gas Mixtures: Dry ATM
Normal Values @ 760mmHg, what happens higher or lower in altitude
-Atmospheric P at sea level; 760mmHg, 760 Torr, 1 atm
-Partial Pressure = Total Atm P x [gas]
-In order to get gas into the body, we need two factors:
1. Gas
2. Pressure
[N2] = 79%
[O2] = 21%
[CO2] = 0.04%
Concentration is also expressed as “F”
This should total 100%, creating a total pressure of 760mmHg.
If higher in elevation, the total pressure should be lower.
If lower in elevation, the total pressure should be higher
[gas] really should remain the same, regardless of altitude, the total pressure of the atmosphere will be less. P partial numbers will be affected
Inspired Gas Pressures
Partial Pressures of Gas Diluted by Water Vapor
-Dry Atm (760mmHg) at 37c
-100% H2O saturation of the gas @ 37 C has a pressure of 47.0mmHg
-Should remain exactly the same no matter what
-This displaces the other gases as we inspire (except CO2)
Inspired Gas at 1atm:
PI O2 : 149mmHg
PI CO2 : 0.3mmHg
PIN2: 564mmHg
P pressure of each gas + water vapor equation:
PI O2 = FI O2 (P B - P H2O )
No way to avoid inspired water vapor. It always happens.
What happens to partial pressures as we inspire air?
Inspired Humidified Gas
- Inspiring fresh air:
PO2 (149mmHg) + PCO2 (0mmHg) - Air then mixes with the 3L of air that remains in the lungs –>
P A O2 (104mmHg) +
P A CO2 (40mmHg)
-O2 concentration increases, CO2 concentration is diluted
PO2 (pulmonary arterial blood, deoxygenated venous blood) has a PO2 of 40mmHg
PCO2 is 45mmHg
- O2 is absorbed into the pulmonary capillaries, and CO2 is unloaded into the alveolar air.
PvO2 increases to 104mmHg
PvCO2 decreases to ~ 40mmHg
As blood is ejected into the L. atrium, the oxygenated pulmonary venous blood mixes with blood in the bronchial circulation, slightly diluting PaO2 (systemic) to ~100mmHg (A-A gradient)
Average Alveolar Pressures at 1atm (After Equilibration)
P A O2: 104mmHg
P A CO2: 40mmHg
P A N2: 569mmHg
P A H2O: 47mmHg
Nitrogen remains ~ the same because our body does not use it in the gas exchange process
Why is PAO2 higher than PaO2?
Alveolar-Arterial Gradient
How do the bronchiol tissues receiver nutrients?
- Oxygen Enters the Alveoli – When you breathe in, oxygen fills the alveoli in your lungs. The partial pressure of oxygen (PAO₂) in the alveoli is high.
- Oxygen Diffuses into Blood – Oxygen moves from the alveoli into the pulmonary capillaries, binding to hemoglobin in red blood cells.
- Mixing with Deoxygenated Blood – Some venous (deoxygenated) blood from the bronchial circulation and thebesian veins enters the systemic arterial circulation. This blood has a lower oxygen content.
-the bronchial tissues receive about 1% of systemic arterial CO in order to deliver nutrients - Slight Drop in Oxygen Content – Because of this mixing, the oxygen content in the systemic arteries is slightly lower than in the alveoli.
-This also means that P v O2 is slightly higher than P a O2
This difference is called the alveolar-arterial (A-a) gradient and is normal.
As a result of aging (>20yrs), what is a normal PaO2?
80mmHg
Increases in ventilation/perfusion (brief summary of how that would change partial pressures)
If ventilation is increased, but pulmonary blood flow remains the same, we would expect to see a high PAO2 and lower PACO2
If pulmonary blood flow is increased, but ventilation remains the same, we would expect to see a lower PAO2 and higher PACO2
How does PPV affect this?
Dead-Space Ventilation; Inspiration
In a 0.5L Vt, the first 350cc of air will make it into the lungs to participate in gas exchange.
-This 350cc mixes with the remaining 3L of air in the lungs and is diluted quite a bit
The remaining 150cc of inspired air does not make it into the lungs for gas exchange. The gas concentration remains unchanged.
-This is called dead-space ventilation. This amount of air is required to push the first 350cc deep enough into the lungs in order for gas exchange to occur
-The upper airway where this takes place is referred to as anatomical dead-space.
-Dead space within the lung is referred to alveolar dead-space (this is pathologic). PPV can cause this overtime
The term physiologic dead-space refers to both anatomical dead-space ventilation and alveolar dead-space.
A normal physiologic dead-space in a perfectly healthy person is 150ml.
Vt, VA, VE Equations
Vt = V D + V A
-Alveolar dead-space & anatomical dead-space fall under V D
Minute Alveolar Ventilation:
V A = V E - V D
-V E : Total minute ventilation (dead-space and alveolar)
to calculate each variables minute volume, multiply each by number of BPM
Normal Minute Values:
V A : 4.2L/min
V D : 1.8L/min
Adding the two together gives us minute Vt
Vt=V E = Vt x BPM
What happens to the gas concentrations of both volumes of air?
Dead-Space Ventilation; Expiration
-Gas composition of the 150cc of anatomical dead-space inspired air will remain relatively unchanged and consistent with the inspired atmospheric air. Remains very concentrated
-The remaining 350cc of the expired breath will be what was mixed with the 3L of air already in the lungs
-Upon expiration of the full 500cc, the air is significantly less concentrated than what was initially inspired
What is the correlation between VA and PAO2 that is graph is showing?
Normal V A : 4.2Lmin
-This correlates with a P A O2 of 104mmHg
As V A increases, we see an increase in P A O2 to a certain point
As V A decreases, we will see a steep decrease in P A O2
This is the pattern if all other factors remain unchanged
Correlation between VA and PACO2?
As we increase V A , P A CO2 should decrease to a certain point
As we decrease V A , P A CO2 will dramatically increase
This is the pattern if all other factors remain unchanged
NFP? Forces that favor reabsorption/filtration?
Pulmonary Starling Force Values
Role of lymphatic system here?
P CAP: 7mmHg
π is : 14mmHg
- ~ double the value of the systemic circulation
P is : -8mmHg
-This is more (-) than systemic circulation because of the negative pleural pressure in the lungs
All three of these forces favor filtration (29mmHg)- movement of fluid out of the pulmonary capillaries and into the interstitium
π pl: 28mmHg
-this is the force that favors reabsorption of fluid back into the capillary
NFP of +1mmHg
Lymphatic system within the lungs is pretty active. PPV or any obstruction can prevent this system from working properly
Pressure that can cause this?
Edema Formation in the Lung
L.AP is normally ~2mmHg
L.AP can usually rise to ~ 23mmHg before edema formation starts in the lungs
How to find NFP, Kf
Net Filtration Pressure = (Pc - Pi + πi) -πpl
If the result is positive → fluid moves out of capillaries.
If the result is negative → fluid moves into capillaries.
To find the Kf, we need to rearrange the equation
Kf= Qf /(Pc - Pis) - (πc - πpl)
Or simply: Kf = Qf / NFP
Qf is measure in volume/time
What is it? 2 factors it relies on? What does a high or low Kf mean?
Pulmonary Kf
Conditions that cause a high/low Kf
Kf in the lungs tells us how easily fluid moves across the capillary walls. It depends on two key factors:
Capillary Permeability – How “leaky” the capillary walls are
Capillary Surface Area – More surface area means more filtration
High Kf tells us: Capillary permeability and/or capillary surface area have increased. End result= pulmonary edema, less oxygenation taking place
Conditions that cause this:
-Inflammation
-ARDS
-Toxin inhalation
-Lung Injury
Low Kf tells us: Capillaries are less permeable or surface area has decreased. End result = less fluid movement, less surfactant transport, impaired clearance of metabolic waste products
Conditions that cause this:
-Pulmonary fibrosis
-Chronic hypoxia
-Emphysema
-Pulmonary HTN
Increase capillary perm, increased Pcap, decrease Pis
Pulmonary Edema & Starling Forces
Decreased πpl
Increased capillary permeability:
-ARDS
-O2 toxicity
-Inhaled toxins
Increased P CAP :
-Increase L.AP from LV MI or mitral stenosis
Decreased P is :
-Rapid evacuation of pneumo or hemothorax (stripping a chest tube)
-Generating massive (-) intrapleural pressure (emergence; inhaling deeply against a closed airway)
-Typically happens in a young, healthy person
Decreased π pl :
-Protein starvation
-Overadministration of fluids, dilution of plasma proteins
-Renal problems resulting in proteinuria
Insufficient pulm lymphatic drainage, unknown etiology
“Other” Causes of Pulmonary Edema
Insufficient pulmonary lymphatic drainage:
-Tumors
-Pulmonary fibrosis
-PPV
Unknown etiology:
-High-altitude pulmonary edema
-Neurogenic pulmonary edema after head injury
-Massive loss of SNS, too much pulmonary blood flow
-Drug overdose
Factors that affect the normal V/Q pattern in apex & base of lung
Ventilation/Perfusion Pattern of the Lung
Perfusion of the lung is gravity dependent.
Apex of the lung has:
-Lower intravascular pressures
-Less recruitment and distention
-Pulsatile perfusion
-Higher resistance –> less blood flow
Base of the lung has:
-Higher vascular pressures
-More recruitment and distention
-Continuous perfusion
-Lower resistance –> greater blood flow
Ventilation should follow perfusion. This gives us a good V/Q match
Apex of lung:
-More negative intrapleural pressure
-Larger transpulmonary pressure difference
-Larger, less compliant alveoli
Base of lung:
-Less negative intrapleural pressure
-Smaller transpulmonary pressure difference
-Smaller, more compliant alveoli
What is happening with alveolar compliance at FRC? Affects ventilation?
Pulmonary Ventilation at FRC
Why does the -Pip at the apex matter? effect on alveoli?
-Apex of the lung has a P IP of -8.5cmH20
-P TP here is: +8.5cmH2O
-Base of lung has a P IP of -1.5cmH2O
-P TP here is: +1.5cmH2O
-Assuming that P A here is 0cmH2O
-Avg pressure inbetween breathes is -5cmH2O, but there is a pressure gradient between the apex and base of the lung
-this gradient causes varying degrees of fullness in the alveoli
-Because the P IP is at it’s most negative at the top of the lung, that pressure is pulling the alveoli open, causing them to fill to nearly 60% capacity with air
-Base of the lung has a lower P IP . Alveoli is pulled open slightly, but are only filled to ~25% capacity.
Air follows the path of least resistance. Air will mostly flow into the alveoli at the base of the lung because alveolar compliance will be at it’s highest there
Slope of curve indicates level of compliance
Ptp & lung volume in relation to alveolar compliance
In general,
As P tp increases, alveolar compliance decreases
As lung volume increases, alveolar compliance decreases
As P tp decreases, alveolar compliance increases
As lung volume decreases, alveolar compliance increases
2 factors important in hysteresis?
Hysteresis- What is it, and where is it shown on this graph?
Hysteresis in the lungs refers to the difference in lung compliance during inspiration and expiration. In simple terms, the lungs don’t inflate and deflate in exactly the same way—more pressure is needed to inflate them than to deflate them.
How does this happen?
- Surfactant Effects
During inflation, alveoli are small at first, and surface tension is high. More transpulmonary pressure (Ptp) is needed to open them.
As lungs expand, surfactant spreads out and reduces surface tension, making further inflation easier. - Tissue Elasticity
Lung tissue resists expansion at first but stretches over time.
During expiration, elastic recoil helps the lungs return to their original shape more easily, meaning, lungs are more compliant during expiration
The difference between the inspiratory & expiratory curve on this graph refers to hysteresis.
What is the compliance at the base of the lung here? How does it change?
Pulmonary Ventilation at RV
Why does ventilation at RV matter to us?
At Apex:
-P ip is -2.2cmH2O
P tp is +2.2cmH2O
At Base:
-P ip at base is +4.8cmH2O
-P tp at base is -4.8cmH2O
Ptp of +2.2cmH2O allows the alveoli to fill to ~ 30% capacity. Alveoli have a higher compliance here
Ptp of -4.8cmH2O, the alveoli in this area will be as empty as they can be; ~20% capacity
-will have collapsed alveoli here
-Alveoli have no compliance. Once the alveoli accept volume, compliance will increase
Air will more easily flow into the apex of the lung here.
As the alveoli in the apex fill, the airways in the base of the lung will be pulled open, allowing for air to fill the alveoli
Why does ventilation at RV matter to us?
-When placing someone under general anesthesia, paralyzing them, and laying them on their back, the patient will have very, very low lung volumes (similar to RV)
2 types of smooth muscle that play a role here?
Hypoxic Pulmonary Vasoconstriction
Which smooth muscle set affects perfusion? Which affects V?
-
Pulmonary Blood Vessel Smooth Muscle
-Have the ability to constrict and relax the pulmonary blood vessels upstream of the alveolar capillaries
-Behaves in the same manner that systemic vascular smooth muscle does -
Airway Smooth Muscle
-Functions to direct ventilation or perfusion to where it will be most useful
Causes of HPV; Pulmonary Smooth Muscle
1. P A O2 is low–> causing vasoconstriction in the extra-alveolar pulmonary vessels, directing blood flow to areas of the lung that are not hypoxic
2. P A CO2 is high –> results in vasoconstriction in the extra-alveolar pulmonary vessels. This is secondary to hypoxia
Causes of HPV; Airway Smooth Muscle
1. P A O2 is high/resembles inspired air partial pressures (~150mmHg) –> airway smooth muscle constricts, directing ventilation to parts of the lung that are not hyperoxic
Mechanism and the overall result
How do volatile anesthetics interfere w/ hypoxic pulmonary vasoconstriction?
How does this affect V/Q matching?
- General anesthetics cause K+ channels to open, leading to relaxation of the pulmonary vessel smooth muscle. This impairs the body’s ability to compensate for a V/Q mismatch
- Ventilation-perfusion (V/Q) mismatch: Anesthesia-induced changes in lung mechanics cause a low V/Q mismatch, reducing oxygenation efficiency
Mechanism:
* Volatile anesthetics (e.g., isoflurane, sevoflurane, desflurane) directly impair pulmonary vascular smooth muscle contraction, reducing the effectiveness of HPV.
Result:
* More blood perfuses poorly ventilated lung regions, leading to increased intrapulmonary shunting and hypoxemia.
Conditions that cause this?
Changes to partial pressures when there are underperfused/overventilated alveoli? (High V/Q mismatch)
Partial pressure of PO2 and PCO2 in an underperfused alveoli will resemble that of the inspired air:
PO2 ~150mmHg
PCO2 ~0mmHg
Why?
In an underperfused alveolus, less oxygen is removed by the blood, so the alveolar P A O2 rises toward the inspired air level (~150 mmHg at sea level).
Since CO₂ is delivered to the lungs via blood flow, reduced perfusion means less CO₂ enters the alveolus.
Pulmonary embolism (PE):
A blocked pulmonary artery reduces perfusion, creating high V/Q areas.
Shock or hypotension:
Low cardiac output decreases pulmonary blood flow, increasing alveolar dead space.
Emphysema:
Loss of capillary beds can create wasted ventilation, leading to high V/Q regions.
Conditions that cause this? Thin- what decreases ventilation?
Changes to partial pressures in overperfused/underventilated alveoli?
In a low V/Q region, blood flow is normal or increased, but ventilation is reduced. This means that gas exchange is impaired, and alveolar gases begin to resemble venous blood.
Changes to P A O2
* Since ventilation is reduced but blood flow remains high, less fresh oxygen enters the alveolus to replenish what is being taken up by the blood. P A O2 is reduced to ~40mmHg
Changes to P A CO2
* With impaired ventilation, less CO₂ is exhaled, leading to an increase in P A CO2 to ~40-45mmHg
Airway obstruction (e.g., mucus plugging, asthma, COPD):
Prevents adequate ventilation, causing local hypoxia.
Pulmonary edema, ARDS, or pneumonia:
Fluid or inflammation in the alveoli reduces ventilation while perfusion remains intact.
Atelectasis (alveolar collapse):
No ventilation occurs in collapsed lung regions, causing a low V/Q, or if no perfusion is also happening, a V/Q= 0, mimicking a true shunt.
Changes in Lung Capacity, V/Q Matching, and Pulm Blood Volume During Upright-Supine Position Changes
Upright to Supine:
Diaphragm Elevation:
* When lying supine, the abdominal organs push the diaphragm upward, reducing available lung space.
* This compresses the bases of the lungs, reducing FRC and ERV.
* IRV is slightly expanded because the lungs begin from a lower volume, allowing for greater inspiratory expansion during deep breathing.
Increased Pulmonary Blood Volume:
* In a supine position, venous return to the thorax increases, leading to increased pulmonary capillary blood volume.
* Increased pulmonary blood volume in supine stiffens the lung parenchyma, making passive expiration (ERV reduction) easier.
* This allows a greater proportion of lung capacity to be used for inspiration, increasing IRV.
Changes in Regional Ventilation-Perfusion (V/Q) Matching:
* In the supine position, the posterior lung regions become more perfused, leading to better V/Q matching in the dorsal areas.
TLC is relatively unchanged, just redistributed
How does it work? What does it measure?
Basic Spirometry
* Upside-down, air-filled bell sitting in a pool of water
* Expired air causes the bell to move upward
* Inspired air causes the bell to move down
Measures Vt, IRV, ERV (vital capacity)
Cannot measure any capacity that has RV included.
- Vital Capacity
- Maximal inspiration
- Inspiratory reserve volume
- Inspiratory capacity
- Expiratory reserve volume
- Maximal inspiration
What 3 things are needed to perform advanced spirometry?
How is this technique done? How can we find FRC & RV?
- This technique uses an inert gas (such as helium, nitrous oxide, or argon) because it is neither absorbed by the body nor metabolized by the lungs.
Need 3 things:
Helium meter, CO2 absorbant, O2 source
- The patient begins by breathing a known concentration of an inert gas (e.g., helium) that is mixed with oxygen.
- The patient breathes normally (tidal breathing) through a closed system, allowing helium to mix with the air in the lungs.
- Over several breaths, helium distributes evenly throughout the lung airspaces.
- Once equilibrium is reached, the final helium concentration in the spirometer and lungs is measured.
FRC can be calculated: C1 x V1= C2 (V1 +FRC)
C: Concentration
V: Volume
RV can be calculated: FRC-ERV
Inert Gases
Usually noble gases
1. Helium- Cheap
2. Neon- Expensive. Not usually done
3. Argon- Levitzsky text used this. Rare. Expensive
4. Xenon
5. Radon- Natural radon on the periodic table is not reactive. Radon found in the ground is very reactive. Have your basements checked. Second leading cause of lung cancer
- Obstructive lung disease:
* Loss of elastic tissue in the lungs. Alveoli are more stretchy —> loss of elastic recoil pressure. More compliant than normal. Requires much lower Ttp to fill the lungs to a high volume. Results in air trapping because elastic recoil is poor during exhalation - Normal
- Restrictive lung disease:
* Less compliant. Requires a much higher Ttp to fil the lungs, and usually they are filled to a lesser volume than normal.
Can take TLC-RV to find VC
When volume is on the side axis and pressure on the bottom axis, the slope of the line measures compliance
What is it? Area within the loop means what?
Hysteresis
How does surface tension apply?
- Hysteresis refers to the phenomenon where the lung’s pressure-volume (PV) relationship differs between inspiration and expiration.
- In other words, at the same transpulmonary pressure, the lung volume is greater during expiration than during inspiration.
- This means that more pressure is required to inflate the lungs than to deflate them, creating a lag between the inspiration and expiration curves on a pressure-volume graph.
- During inspiration, the lungs must overcome elastic recoil and airway resistance –> lag between curves. As lungs expand, surfactant spreads out and reduces surface tension, making further inspiration easier.
- During expiration, the stored elastic energy assists recoil, making expiration require less effort.
- This creates a loop-shaped curve, where the area within the loop represents the work of breathing.
Factors/Conditions That Affect Hysteresis
- Mechanical Ventilation
* In ARDS (Acute Respiratory Distress Syndrome), hysteresis is more pronounced due to surfactant dysfunction and stiff lungs.
- PEEP (Positive End-Expiratory Pressure) is used to keep alveoli open and reduce hysteresis.
- Lung Disease
* Restrictive Lung Disease:
Narrower loop, flatter slope → Less hysteresis because these lungs are stiff and have less alveolar recruitment/derecruitment.
Higher pressures are needed to achieve the same volume.
- **Obstructive Lung Disease **
Steeper slope, Wider loop → Greater hysteresis due to air trapping and delayed expiration.
Larger lung volumes due to high compliance (floppy lungs).
Surfactant controls what? Lipids that make up surfactant? Proteins?
Surfactant
% of lipids? % of proteins? How is surfactant oriented?
- Surfactant controls how much surface tension there is in the lungs
- Breaks surface tension.
- Surfactant orients hydrophillic head inbetween water molecules, point the lipid tail backwards preventing the molecules from sticking together
- Compounds that make-up surfactant:
- Lipids
- phosphatidylglycerol, phosphatidylinositol- 9%
- phosphatidylserine, phosphatidylethanolamine, sphingomyelin- 6%
- Dipalmitoylphosphatidylcholine- 31%
- Unsatured phosphatidylcholine- 31%
- Amphipathic- meaning they are both water and lipid/oil soluble
- Proteins; four proteins
- SP-A, SP-D; hydrophillic
- SP-B, SP-C; hydrophobic
Macrophages, mast cells
- Clara Cells:
- (Club cells). Secretory cells that line the lower airway, secrete surfactant.
- Clara was the last name of a nazi that did bad things
- Type II Alveolar Cells:
- Secretory cell. Produce surfactant. Interspersed inbewtween the Type I cells in the alveoli.
- Type II cells are shaped like a cube in order to contain nucleus…etc inside
- 5-10% of surface area in lungs
- 2x as many as Type I
- Type I Alveolar Cells:
- Thin, gas exchange cells
- Makeup 90-95% of gas exchange surface area
- Tubular myelin
- Located directly under water layer
- Surfactant is exocytosed and stored on the tubular myelin
- Negative alveolar pressure and mechanical stretch during inspiration causes surfactant to be released from this netting.
- PPV can release some surfactant, but does not work as well as negative pressure ventilation
- Air-water interface
- This is where surfactant becomes active and reduces surface tension
- Goblet cells:
- Secretory cells located in the upper airways. Secretion of mainly mucus and some surfactant
Surfactant falls apart overtime and are digested by alveolar macrophages –> breaks it down into component parts that are recycled by Type II and Club cells
Mast cells: Release histamine and inflammatory mediators after injury
Atelectasis, Surfactant, & Recruitment
- When alveoli collapse, the type II alveolar cells, which produce surfactant, may become damaged or less active.
- This reduces surfactant secretion, making it harder for alveoli to reopen.
- Additionally, poor lung expansion decreases the mechanical stretch that stimulates surfactant production. Over time, this creates a cycle where reduced surfactant leads to more alveolar collapse, worsening atelectasis.
- The longer the lung is collapsed, the harder it will be to re-recruit that portion of the lung
How many sq meters of gas exchange tissue?
How many alveoli in a young, healthy adult? How many capillaries in each?
Can you grow new alveoli?
- 500million alveoli as young adults
- Each alveoli can contain up to 1,000 capillaries
- 70 square meters of gas exchange in the lungs (size of a tennis court)
- Lungs can produce new alveoli, complicated, slow process.
- If you have one lung removed at the age of 20, possible to grow new alveoli
- Chronic illness, probably not
Elastic recoil depends on what 2 factors?
Elastic Recoil & Surface Tension
Changes to elastic recoil & surface tension w/ chronic conditions
- Alveoli have a tendency to recoil on themselves (elastic recoil pressure)
- Elastic recoil depends on
1. Elasticity of the tissue (1/3rd)
2. Surface tension (2/3rds) - Surface tension is the force within the alveoli that wants to bring the water lining the alveoli as close together as possible
- This causes alveoli to recoil in, pushing air out of the lungs
Changes in chronic conditions:
Restrictive lung disease:
More elastic tissue
Higher surface tension
More tissue resisting filling of the alveoli
Obstructive lung disease
Less elastic tissue
Uneven surface tension
Less tissue resisting filling of the alveoli
Every lung disease ever studied has what kind of deficiency?
Surfactant
Small airways vs large airways
Airways resistance & lung volume
As lung volume increases, alveoli are stretched out, and airway diameter increases in small airways (lower airways resistance)
* this allows for easier/faster exhalation
Large airways:
* Decreased P pl causes more traction on the airways, pulling them open
As lung volume decreases, alveoli are less stretched out, and airway diameter decreases (higher airways resistance)
* this can limit the speed at which we an exhale
Dead Space vs Shunt
Dead Space:
Ventilation is occuring, but little to know perfusion is happening. This means there is poor or no gas exchange. This leads to a high V/Q
Shunt:
The area is perfused, but not ventilated, also resulting in no gas exchange. A true shunt has a V/Q of 0
Pulmonary Compliance Equation
Delta V/ (End inspiration PA-Pip) - (Preinspiration PA-Pip)
Total Pulmonary Compliance
Delta V/ (End of inspiration PA-Pb) - (Pre inspiration PA-Pb)
Units: L/cmH2O
Total Compliance Equation Including CW complaince
1/total compliance = (1/pulmonary compliance) +(1/cw compliance)
PNS/SNS & Airways Resistance
Stimulating PNS: Constricts airway –>increased airway resistance
Stimulating SNS: Relaxes airway —> decreased airway resistance
What happens to lung capacities/volumes as we age?
- Loss of elastic recoil
* This causes FRC and RV to be increased
* ERV is decreased
FRC Equation for Advanced Spirometry
C1 x V1= C2 (V1 or V2,if given, + FRC)
Bohr Equation
VDCO2/VT= PaCO2- PECO2/PaCO2
New CO2 Based on Changes in VA
New CO2 = VA (old) / VA (new)
