Pulm; Exam III Flashcards

Question

# PFT to determine Steps 2, 3, 4, & 5?

Answer 1

Step 2: NO washout Step 3: He Dilution Step 4: Carbon minoxide dilution Step 5: Administer bronchodilator

Answer 2

**X** * FEV1 is 4L * FVC is 5L * FEV1/FVC = 80% **Z** * FEV1 is 3L * FVC is ~3.5L * FEV1/FVC = ~85% Apparently the second graph is indicating different efforts/breaths

Answer 3

Closing capacity is the lung volume at which small airways begin to close during expiration, especially in the dependent (lower) regions of the lungs (because the patient expires down to RV)

Answer 4

* Patient expires down to RV * Starting PN2 at RV is 569mmHg (uniform throughout lung) * Base of the lung is collapsed (filled to 20% capacity) -More new air will fill the base of the lung -Adding 80% of the alveoli's capacity to bring them to TLC -PN2 will be more diluted here than the apex when inspiring 100% O2 * Apex of the lung is relatively empty (filled to 30% capacity) -Adding 70% of the alveoli's capacity to bring them to TLC -PN2 will be less diluted here because less air is filling this area of the lung

Answer 5

**Closing Capacity/Volume Test** * Measured using a test called the Single-Breath Nitrogen Washout Test: * Tells us at which volume our small airways collapse * Instruct the patient to forcefully exhale down to RV * The patient inhales 100% oxygen from RV to TLC. * Then they slowly exhale back down to RV while exhaled gas is analyzed for nitrogen content. * The nitrogen concentration vs. exhaled volume gives a curve with four phases. **A. Phase I:** * Expiration of dead space air. Should not contain any N2 (for ~100ml) **B. Phase II:** * Transitional phase. Anatomical dead space air is mixed with some alveolar air--> expired N2 increases throughout phase II. *This is what the Fowler test measures* **C. Phase III:** * Alveolar plateau. Initially, this gas comes mostly from the lower, dependent alveoli that were: -Well ventilated (full of O₂, higher % of N₂ dilution) -Last to fill, so first to empty * As exhalation continues, lung volume decreases, and gas from apical regions (less ventilated & more nitrogen-rich) begin to appear, contributing to the upward slope of Phase III. **D. Phase IV:** * Toward the end of expiration, nitrogen concentration suddenly rises sharply. This marks the point when small, dependent airways at the base of the lung begin to close, and alveoli in those areas empty nitrogen-rich air. 1. Point at which CC starts 2. Closing volume 3. Point at which RV starts 4. Residual Volume 5. Closing Capacity: CV + RV

Answer 6

**1. Premature airway closure** This results in an early onset of Phase IV → so Phase III appears shortened. Examples: * Obstructive lung disease * Aging (natural loss of airway support) * Smoking-related airway narrowing **2. Increased Closing Capacity** If the CC exceeds the FRC, the dependent airways start closing during normal expiration. This shifts Phase IV to begin earlier, shortening Phase III. This can be due to: * older adults * anesthesia * supine position **3. Reduced alveolar volume** In diseases with reduced alveolar recruitment, the alveolar plateau may be abnormally short due to: * Decreased total lung volume (restrictive lung disease)

Answer 7

* Closing volume changes as we normally age -Airways start collapsing at a higher volume -At age 70, our small airways begin to collapse before we exhale down to FRC due to loss of elastic tissue. This happens w/ every breathe, not just forceful exhalation -Increased WOB * RV increases w/ age --> more difficult to empty the lungs * ERV decreases due to increase in RV * Other capacities remain relatively the same volume as we age and have healthy lungs

Answer 8

**Solubility coefficient of O2:** * 0.003ml O2/ mmHg PO2/dL * What does this mean? For each 1mmHg of PO2 in the environment, 0.003ml O2 can be dissolved in 100ml solution **Dissolved Oxygen** * The amount of O2 dissolved in the plasma, not bound to Hb * Dissolved oxygen in your blood is a reflection of the PO₂ in the air around your lungs. * The dissolved oxygen in the blood creates its own partial pressure. * That pressure opposes further diffusion of oxygen in—until both sides are balanced (equilibrium) **How do we solve for dissolved O2 content?** Dissolved O2 Content (ml O2/dL) = (0.003ml O2/dL x mmHg) x PO2 in mmHg Under normal circumstances: Arterial dissolved O2 content: 0.3ml O2/dL --> 0.003ml O2/dL x 100mmHg Venous dissolved O2 content: 0.12ml O2/dL ---> 0.003ml O2/dL x 40mmHg

Answer 9

250ml O2/min

Answer 10

**Oxygen Carrying Capacity of Hb:** * 1.34ml O2/ gram of Hb (this is a constant) * Normal Hb: 15g/dL * 15g/dL x 1.34ml O2/g Hb = 20.1 ml O2/dL blood Arterial: 20.1ml O2/dL blood would be 100% Hb saturation (with this Hb level) If we had an Hb saturation of 60% --> multiply the total number by 0.6 Venous: 20.1ml/O2 x 75% saturation = 15.08ml O2/dL blood

Answer 11

**HbA or A Hb** * Adult Hb * Tetromer: two alpha subunits and two beta subunits * The combination of these subunits can carry four O2 molecules **Fetal Hb or HbF** * Tetromer: two alpha subunits and two gamma subunits * Significantly higher affinity for O2 than HbA

Answer 12

* In the placenta, oxygen moves from the mother’s blood to the fetal blood. * For that to happen, HbF has to "grab" oxygen more tightly than the mother’s hemoglobin. **Binds less strongly to 2,3-BPG** * This molecule normally binds to adult hemoglobin (HbA) and reduces its affinity for oxygen—helping it release oxygen to tissues. * Fetal hemoglobin (HbF) binds less strongly to 2,3-BPG. * That means 2,3-BPG doesn’t push oxygen off HbF as easily, allowing HbF to hold onto O2 more tightly --> L. Shift

Answer 13

* EPO * Released from kidneys in response to low oxygen

Answer 14

* Structurally similar to HbA * Has a higher affinity for oxygen * Its job is to store oxygen and release it during intense muscular activity * Myoglobin’s high affinity ensures it won’t release O₂ until oxygen levels are very low

Answer 15

Dissolved content + bound content= Total content

Answer 16

**When CO binds to Hb:** * Total O2 content decreases because carrying capacity of Hb decreases * Dissolved O2 content remains the same * PaO2 will remain the same or relatively unchanged * SPO2 will be falsley normal * CO increases Hb's affinity for oxygen (left-shift) meaning: 1. Hemoglobin holds onto oxygen more tightly 2. Oxygen is less likely to be released to tissues

Answer 17

* Anemia= reduced hemoglobin concentration → less oxygen-carrying capacity. * PaO₂ may still be normal, but total O₂ content is lower. * The body needs to compensate to deliver more oxygen to tissues (lower affinity for O2) **How does the body compensate?** 1. Anemia triggers the body to produce more 2,3-BPG in red blood cells. * 2,3-BPG binds to hemoglobin and reduces its affinity for O₂, promoting oxygen release. 2. Anemia → less O₂ delivered → mild tissue hypoxia * *This may cause:* * Increased CO₂ (shifts curve right via Bohr effect) * Increased H⁺ (lower pH) from anaerobic metabolism * Increased temperature **All of these promote O₂ unloading—another way to shift the curve right**

Answer 18

O2 bound to Hb / O2 Capacity of Hb x 100% *Where "Carrying Capacity" = 1.34ml O2/ gram Hb* 1.34 x Hb x HbSat = O2 Bound * Venous Hb is only ~3/4ths saturated (75%) * Arterial Hb is close to 100% saturated

Answer 19

* The heart * Hb that flows into coronary circulation is saturated normally * Venous blood exiting the coronary circulation through the coronary sinus has a v Hb sat of 25% (in comparison to normal V. Hb sat of 75%) * This means the heart is extracting 75% of the O2 that is circulated through the coronary circulation --> very efficient, cuts down on the amount of coronary perfusion needed * Downside: Very little room for error if blood flow is affected

Answer 20

* Describes the relationship between PO2 at HbSat * As PO₂ increases, Hb saturation increases **Increased affinity → Left shift** * Hemoglobin holds onto O₂ more tightly * Harder to unload O₂ to tissues * This means that a lower PO2 is required to allow for the same Hb saturation as Hb w/ a lower or normal affinity **Decreased affinity → Right shift** * Hemoglobin releases O₂ more easily. * Facilitates O₂ delivery to tissues * Will see a higher PO2 level here --> Hb is more willing to release O2 **Example:** * HbF only requires a PO2 of ~18mmHg to aquire 50% HbSat due to its increased affinity * HbF only requires a PO2 of ~30mmHg to aquire 100% HbSat * HbA requires a PO2 of ~28mmHg to aquire a 50% HbSat * HbA requires a PO2 of ~100mmHg to aquire 100% HbSat

Answer 21

* Volumes % indicates O2 content if Hb is normal (15g/dL)

Answer 22

*Explains how CO₂ and pH affect hemoglobin's affinity for oxygen.* When tissues are active, they produce: * More CO₂ * More H⁺ ions (↓ pH) These changes shift the oxygen dissociation curve to the right, meaning: * Hemoglobin lets go of O₂ more readily (decreased affinity) * More O₂ is delivered to where it's needed This is the Bohr effect in action.

Answer 23

**Example of the Bohr Effect** 1. ↓ CO₂ shifts the curve to the left --> O2 is more prone to "hold on." 2. Normal conditions 3. ↑ CO₂ shifts the curve to the right --> more O2 is prone to unload, dissolve, and be distributed to the tissues

Answer 24

**Example of the Bohr Effect** 1. ↑ pH → ↑ O₂ affinity → O₂ held tightly → Left shift -Usually accompanies a ↓ CO₂ 2. Normal conditions 3. ↓ pH → ↓ O₂ affinity → O₂ released → Right shift -Usually accompanies a ↑ CO₂

Answer 25

**Bohr** 2,3-BPG is a byproduct of metabolism. The higher our metabolism --> the ↑ 2,3-BPG is * 2,3 Bisphosphoglycerate * 2,3 Diphosphoglycerate * Bisphosphoglyceric acid 1. ↓ 2,3-BPG ↑ O₂ affinity → O₂ held tightly → Left shift 2. Normal 3. ↑ 2,3-BPG ↓ O₂ affinity → O₂ released → Right shift

Answer 26

**Bohr** 1. Decreased temp: ↑ O₂ affinity → O₂ held tightly → Left shift 2. Increased temp: ↓ O₂ affinity → O₂ released → Right shift Temperature in the lungs is usually 37. Temperature is slightly increased in the tissues to facilitate O2 unloading at the tissues and O2 loading in the lungs

Answer 27

* PCO₂ is lower than PaCO2 because CO₂ is being exhaled * pH is higher * Temperature is cooler **These conditions increase hemoglobin’s affinity for O₂.** Result: O₂ binds more readily to hemoglobin → O₂ loading.

Answer 28

**Conditions in healthy venous blood** * Higher PCO2 * Lower pH * Lower SvO2 than SaO2 * Slightly shifted to the right in comparison to arterial

Answer 29

**P50 Value** * Describes the PO2 required to obtain a HbSat of 50% * Shifts as Hb affinity for O2 changes * Normal P50: 26.5mmHg * R. Shift: Will require a higher P50; *meaning, we will need a higher amount of dissolved O2 in order to increase the PO2* * L. Shift: Will require a lower P50 *meaning, we will need a lower amount of dissolved O2 in order to decrease the PO2*

Answer 30

**Dissolved CO2** * 0.06ml CO2/mmHg/dL blood x PCO2 mmHg = dissolved CO2 content * Makes up 5% of CO2 content **Arterial blood:** * 0.06ml CO2/mmHg/dL x 40mmHg = 2.4ml CO2/dL blood **Venous blood:** * 0.06ml CO2/mmHg/dL x 45mmHg= 2.7ml CO2/dL blood

Answer 31

**Carbamino CO2** * Carbamino compound (CO2) replaces an H+ ion on a terminal amine group * H+ falls off --> dissociates into solution * Represents 5% of CO2 carried in the blood * 2.4ml/dL

Answer 32

Accounts for 90% of CO2 carried through the blood CO2 +H2O ⇌ H2CO3 ⇌ H +HCO3− The environment determines which way the equation shifts. ↑ CO₂ --> Equation shifts to the right ↓ CO₂--> Equation shifts to the left

Answer 33

1. Carbamino group increases to ~30%. More CO2 in venous blood = more carbamino groups 2. HCO3- decreases. Venous blood is more acidic --> ↑ H⁺ 3. Dissolved content increases because PCO2 is higher in venous blood *Understand this concept, but do not need to use these numbers when calculating CO2 content in our class*

Answer 34

Dissolved + Carbamino + HCO3- = Total CO2 Content If dissolved/carbamino make up 5% total CO2 each--> total CO2 should be 48ml CO2/dL blood

Answer 35

Describes how the presence of oxygen affects CO₂ transport in the blood. **In the Tissues (Low O₂, High CO₂):** * Hemoglobin releases O₂ → becomes deoxygenated. * DeoxyHb: -Binds more CO₂ (forms HbCO₂). -Buffers H⁺ ions * Result: *More CO₂ is carried in blood as bicarbonate and carbaminohemoglobin.* **In the Lungs (High O₂, Low CO₂):** * Hemoglobin binds O₂ → becomes oxygenated * HbO₂: -Releases CO₂ (reduced affinity for CO₂). -Releases H⁺, which drives CO₂ formation from bicarbonate * Result: CO₂ is exhaled.

Answer 36

* Shows the relationship between the partial pressure of carbon dioxide (pCO₂) and the total CO₂ content in the blood * Unlike the oxygen dissociation curve (which is sigmoidal), the CO₂ curve is almost linear. **Why is it linear?** * As pCO₂ increases, more CO₂ dissolves in plasma * More CO₂ is also converted to bicarbonate (HCO₃⁻) via the carbonic anhydrase reaction: CO2 +H2O ⇌ H2CO3 ⇌ H +HCO3− * CO₂ also binds to Hb to form carbaminohemoglobin: CO2 + Hb ⇌ HbCO2 * Combined, these forms contribute to the total CO₂ content—hence, the curve steadily rises as pCO₂ increases.

Answer 37

As PCO2 increases --> Total CO2 Content increases--> Moves the point on the curve upward/towards the right As PCO2 decreases --> Total CO2 content decreases --> moves the point on the curve downward/towards the left * Influenced by oxygen levels. * Higher PO2 means less CO2 can be carried --> this moves the point down/towards the left * Lower PO2 means more CO2 can be carried in the blood --> this would move the point up the curve

Answer 38

**Arterial** PCO2 is 40mmHg --> arterial CO2 content is ~ 48ml CO2/dL **Venous** PCO2 is 45mmHg --> venous CO2 content is ~52.5ml CO2/dL No clean way to do the math for this. Needs to be given to us on a graph. Just remember these are normal *The vertical distance between the two lines at any pCO₂ represents the amount of CO₂ released in the lungs as hemoglobin becomes oxygenated* This illustrates the Haldane Effect 4.5ml CO2/dL unloaded

Answer 39

**Arterial** 20.4ml O2/dL blood **Venous** 15.3ml O2/dL blood The different between these two tells us how much O2 is being loaded in the lungs: 5ml O2/dL loaded

Answer 40

**Peripheral Tissue** * CO2 is produced in the tissue as a product of metabolism **Plasma** * CO₂ dissolves in plasma --> travels into RBC **In the erythrocyte:** * 5% CO2 remains dissolved * CO₂ is converted to HCO₃- via the carbonic anhydrase reaction: 1. CO2 +H2O ⇌ 2. H2CO3 (Carbonic Acid) 3. ⇌ H +HCO3− 4. HCO3- exhanges with Cl- via the HCO3-/Cl- transporter. (HCO3- moves into plasma, Cl- moves into RBC) 5. Cl- remains here until it reaches the lungs * HHb buffers H+ released from HCO3- production * 5% CO₂ binds to HHb (or any other plasma protein) to form a carbamino compound * HbO2 unloads inside the RBC due to the decrease in pH ---> O2 diffuses into tissue Result: O2 unloads, CO2 loads

Answer 41

**In the erythrocyte** * Portion of dissolved CO2 leaves RBC --> plasma --> diffuses into alveolus * Dissolution of carbamino compounds: 1. H+ falls off in this process 2. HCO3- is brought back into the RBC in exchange for one Cl- 3. H +HCO3− ⇌ H2CO3 4. H2CO3 ⇌ H2O + CO2 5. CO2 diffuses into alveolus * Decreased presence of CO2 and H+ facilitates O2 loading from the alveolus --> plasma --> onto Hb

Answer 42

When blood enters the pulmonary capillaries, gas exchange begins immediately **O₂:** Equilibrates with alveolar air in about 0.25 seconds (at rest). That leaves a safety margin—so even during exercise (shorter capillary time), O₂ can still equilibrate unless something goes wrong **CO₂** CO₂ is more soluble than O₂, so it also equilibrates quickly—also within ~0.25 seconds. Despite its slower diffusion rate compared to O₂, its high solubility balances that out. **Pulmonary Capillary Transit Time** * At rest, blood spends about 0.75 seconds in a pulmonary capillary. * During exercise (or significant increase in CO), this can shorten to ~0.25 seconds. * Gases must fully equilibrate within this time; and in a healthy lung, they will

Answer 43

**N2O** *Perfusion-limited gases are limited by how fast blood moves past the alveolus—not by the diffusion rate.* * N₂O doesn’t bind hemoglobin, so it stays dissolved in plasma. * Reaches equilibrium fast * Partial pressure in blood rises quickly and matches alveolar pressure in in less than 0.1 sec * Uptake limited by blood flow * Once equilibrium is reached, only more blood flow (perfusion) can increase uptake. **CO** *Diffusion-limited gases depend on how quickly gas can move across the membrane—not on blood flow.* * Binds hemoglobin extremely tightly * Very little CO remains dissolved in plasma, so the partial pressure stays near zero * Never reaches equilibrium -Even as CO diffuses into blood, the partial pressure doesn’t rise (because it does not remain dissolved in plasma), so diffusion never plateaus * Mirrors diffusion rate of O2

Answer 44

* The DLCO test measures how efficiently the lungs transfer gas from the air (alveoli) into the bloodstream. * Rate of uptake is limited only by the diffusion ability of the lung

Answer 45

* Pulmonary fibrosis: Thickened alveolar membrane * Emphysema: Destroyed alveolar surface area * Pulmonary edema: Fluid in alveolar space impairs diffusion * Pulmonary embolism: Blocked blood flow = less gas uptake

Answer 46

* Gas equilibrates between blood and alveolar air, and blood flow is the only limit to further gas uptake * Gas (N₂O, O₂, CO2 in normal lungs) equilibrates with alveolar air very fast * Once PO2 in capillary = PAO2 in alveolus, no more diffusion happens unless fresh blood arrives. * So gas uptake depends on how much blood passes by (perfusion)

Answer 47

* Gas does not reach equilibrium between alveolar air and blood by the time the blood exits the capillary -->no alveolar plateau *So the rate of diffusion is the limiting factor.* Happens when: The diffusion barrier is thickened (e.g., fibrosis) The gas binds Hb so strongly that its partial pressure stays low (e.g., CO) Diffusion continues the whole time the blood is in the capillary, but never fully equilibrates

Answer 48

Fick's Law of Gas Diffusion Dictates how fast gas will move across a barrier **T:** Thickness of the barrier **A:** Surface area; -Can be dependent on perfusion. Increased perfusion = increased recruitment, distention, and available surface area. Decreased perfusion = decreased recruitment, distention, and available surface area. **D:** Diffusivity **P1-P2:** Delta P

Answer 49

Diffusivity∝ Solubility/ Sq. Rt of Molecular Weight Diffusivity increases when solubility increases, and decreases when molecular weight increases Ex: CO2 is 24x more soluble than O2 even though CO2 is larger Diffusivity of CO2 is 20x that of O2

Answer 50

Anemia = reduced Hb * Reduced O2 carrying capacity--> less total O2 -Dissolved PO2 remains the same * Reduced CO2 carrying capacity in the carbamino compound form -PCO2 may remain the same -More CO2 will have to be carried as HCO3-

Answer 51

A. Normal V/Q = 0.8-0.85 (4200ml/5000ml) **B. Decreased Ventilation --> Decreased V/Q** * Partial pressures will match partial pressures of pulmonary artery. PO2: 40mmHg, PCO2: 45mmHg * Extreme: Shunt * V/Q can be as low as 0 **C. Decreased Perfusion ---> Increased V/Q** * Partial pressures will match that of inspired air. PO2: 150mmHg, PCO2: 0mmHg * Extreme: Alveolar deadspace (PE) * V/Q limit is infinity

Answer 52

**Base of the lung** * Higher blood flow and ventilation compared to the Apex * Blood flow is higher than ventilation at the base * Base is underventilated --> Lower V/Q than average * Lower PO2, higher PCO2 **Apex of the lung** * Lower blood flow and ventilation than the base * Ventilation is higher than blood flow at the apex * Apex is overventilated --> Higher V/Q than average * Higher PO2, lower PCO2

Answer 53

**Base** * PO2: ~90mmHg * PCO2: ~42-43mmHg **Apex** * PO2: ~130mmHg * PCO2: ~30-35mmHg

Answer 54

As alveolar ventilation increases, PAO2 increases As alveolar ventilation decreases, PAO2 decreases

Answer 55

As alveolar ventilation increases, PACO2 decreases As alveolar ventilation decreases, PACO2 increases

Answer 56

* PE * Alveolar Deadspace * Reduced CO/HoTN * Overventilation Ventilation > perfusion

Answer 57

* COPD * Asthma * Pulmonary edema * Atelectasis (can lead to shunt) * Airway Obstruction Perfusion > Ventilation

Answer 58

* Overdistention of the alveoli * Compression of pulmonary capillaries due to overdistention cutting off perfusion * End result: Ventilation, but no perfusion

Answer 59

Just understand the trends caused by age V/Q matching gets worse as we age even if you're entirely healthy

Answer 60

Atelectasis happens almost immediately upon induction of anesthesia and no PEEP

Answer 61

* LaPlace's Law * Pressure is dependent upon radius * Larger radius = lower pressure * Smaller radius = higher pressure **According to this law:** * Smaller alveoli (smaller radius) would need more pressure to stay open. * This means small alveoli would collapse into larger ones because air will leave the higher pressure alveoli and travel into the lower pressure alveoli. * Also predicts that collapsed alveoli would never receive any fresh air **Why doesn't this apply to the lungs?** * Surfactant * In smaller/empty alveoli, surfactant is more concentrated → lower surface tension → easier for air to enter * In large/fuller alveoli, surfactant is more spread out/dilute → higher surface tension * This balances the pressure in alveoli of different sizes so they can coexist without collapsing into each other. *LaPlace's Law does apply if we have a surfactant deficiency --> causing uneven ventilation*

Answer 62

Surfactant

Answer 63

** Stretch is the stimulus for surfactant production and activation** * Type II pneumocytes produce surfactant * These cells respond to alveolar stretch (like during inspiration). * Stretch = mechanical signal to synthesize and release surfactant. * Atelectasis removes the stretch * Type II cells don’t get the “stretch signal.” * → Downregulation of surfactant production. * Surfactant recycling also decreases Normally, surfactant is reused after being reabsorbed. Surfactant falls apart and is not recycled

Answer 64

Combination of all expired gases * PEO2: 120mmHg (115mmHg is what I get) * PECO2: 28mmHg * PEN2: 566mmHg * PEH2O: 47mmHg

Answer 65

Bohr Equation Rearrange to solve for PECO2 PECO2 = PACO2 ( 1- VD/Vt)

Answer 66

PEO2 = [(VD/Vt) x PIO2] + [(1-VD/Vt) x PAO2]

Answer 67

[gas in decimal form] x volume of container

Answer 68

-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

Answer 69

-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.

Answer 70

-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

Answer 71

-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

Answer 72

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

Answer 73

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**

Answer 74

-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)

Answer 75

* **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_Abriefly 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).

Answer 76

-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

Answer 77

-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

Answer 78

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

Answer 79

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

Answer 80

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

Answer 81

The effort independent areas on the right side of the curve

Answer 82

A measure of small airway reactivity

Answer 83

End-tidal CO2 should be equivalent to blood gas values **Phase I (Baseline):** Exhaled air from anatomic dead space (trachea, bronchi) Contains no CO₂ → flat line at 0 **Phase II (Ascending Limb):** Air from mix of dead space + alveoli CO₂ rises quickly **Phase III (Alveolar Plateau):** Mostly air from alveoli CO₂ levels should plateau, but in reality they show a gentle upward slope As exhalation continues, air comes from progressively deeper and slower-emptying alveoli, which often have higher CO₂ levels. CO2 levels also rise throughout expiration because CO2 continues to be offloaded from the blood into the alveoli *So the CO₂ concentration rises slightly throughout exhalation → sloped plateau* **End-Tidal Point:** The peak of phase III This is your EtCO₂ — reflects alveolar CO₂ **When is alveolar CO2 at its lowest point?** When fresh air is introduced into the lungs

Answer 84

* Small airways in the bases collapse early * These CO₂-rich units don’t get to exhale fully * They drop out early in the breath The rest of the breath comes from: * Apical alveoli = less perfused, lower CO₂ content * These stay open longer (due to less collapse) and empty later So over time in the breath: * You’re seeing less and less CO₂ as the low-CO₂ apices contribute more and more to the expired air

Answer 85

Long circuit tubing Ventilator initiates inspiration first, but the response is delayed on the capnograph because the remaining expired gas needs to travel through the circuit tubing

Answer 86

Need a moisture trap in order for ETCO2 to function properly Massively sensitive to humidity Dr. Schmidt had 3 in his lab, 2 were always getting repaired and 1 only kind of worked. ~20k

Answer 87

* Alveolar dead space will not contain any CO2 * Alveoli affected by dead space will empty at the same time as well ventilated alveoli ---> diluting the ETCO2 concentration * ETCO2 < PaCO2 usually indicates alveolar dead space

Answer 88

* Used to calculate VD * Subtract anatomic dead space from total VD = alveolar dead space FECO2 x VT = (FICO2 x VDCO2) + (FACO2 x VA) Vol. of mixed expired CO2 = Vol. of CO2 from dead space + Vol. of CO2 coming from alveoli Volume of CO2 coming from dead space will always be zero. CO2 is only present in ventilated alveoli

Answer 89

Two barriers to air entering the lungs: 1. Lungs 2. Chest wall **Normal Conditions** * Lungs normally want to recoil inward due to elastic recoil pressure (PER, Pel) * At a normal FRC, the chest wall wants to recoil outward * In a sealed setting, the potential inward recoil of the lungs and the outward recoil of the chest wall give us our Ppl of -5cmH2O **Less Elastic Recoil of Lung** * Due to COPD/Emphysema * Chest wall has less pressure opposing it's outward recoil, so chest will begin to protrude outward --> barrel chest * Leads to a higher lung volume at a much lower Ptp * Ppl will increase because recoil forces are out of balance, maybe -2.5cmH2O

Answer 90

Compliance = Delta V/ Delta P Pulmonary Compliance: 0.2 L/cmH2O Chest Wall Compliance: 0.2L/cmH2O Total Lung Compliance: 0.1L/cmH2O The lungs and chest wall are a system in series," meaning that RESISTANCE is additive ( Rtotal= R1 + R2 +...) Compliance is the inverse of resistance; therefore, the equation for total compliance is: 1/Total Compliance= (1/pulm. compliance) + (1/chestwall resistance)

Answer 91

If we lose the integrity of the chest wall, the lung often collapses. Because the lung has lost the outward pulling force of the chest wall, the lung's natural tendency to recoil inward goes unopposed. * Loss of negative Ppl * Chest wall can no longer expand properly, lung cannot inflate * Ppl equilibrates with PB (bad) **Conditions that cause this to happen:** - Pneumothorax, open - Pneumothorax, closed (a ruptured bleb, barotrauma, or penetrating trauma that seals) - Air leaks from the lung into the pleural space - Ppl rises toward atmospheric (or even above) - eliminates the pressure gradient that keeps the lung inflated - Hemothorax - Also causes Ppl to rise to or above PB, eliminating the pressure gradient to hold the lung open - Surgical opening of the thorax - Flail chest (multiple broken ribs)

Answer 92

RV will decrease to <1L